ArticleMolecular medicine reports2022
KLF4 downregulates FGF21 to activate inflammatory injury and oxidative stress of LPS‑induced ATDC5 cells via SIRT1/NF‑κB/p53 signaling.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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19 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
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- Alterations of circulating exosomal microRNAs in an LPS-induced depression model of male mice: Potential role in the anti-depressive effects of acupuncture.Physiological reports · 2025Article
- MASP1 modulation as a novel therapeutic target in severe pediatric pertussis: insights from a multi-omics approach.Infection and immunity · 2025Article
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- Intestinal epithelial Krüppel-like factor 4 alleviates endotoxemia and atherosclerosis through improving NF-κB/miR-34a-mediated intestinal permeability.Acta pharmacologica Sinica · 2024Article
- Involvement of Fgf2-mediated tau protein phosphorylation in cognitive deficits induced by sevoflurane in aged rats.Molecular medicine (Cambridge, Mass.) · 2024Article
- Puerarin attenuates myocardial ischemic injury and endoplasmic reticulum stress by upregulating the Mzb1 signal pathway.Frontiers in pharmacology · 2024Article
- The Mechanism of "Treating Different Diseases with the Same Treatment" by Qiangji Jianpi Decoction in Ankylosing Spondylitis Combined with Inflammatory Bowel Disease: A Comprehensive Analysis of Multiple Methods.Gastroenterology research and practice · 2024Article
- Anti-inflammatory effect ofApplied and environmental microbiology · 2023Article
- MAPK Is a Mutual Pathway Targeted by Anxiety-Related miRNAs, and E2F5 Is a Putative Target for Anxiolytic miRNAs.Biomolecules · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ankylosing spondylitis (AS) is a chronic inflammatory disease. Transcriptional regulation of fibroblast growth factor 21 (FGF21) by the transcription factor Krüppel‑like factor 4 (KLF4) serves an important role in chronic inflammatory disease. However, to the best of our knowledge, the role of both these factors in AS has not been previously reported. In the present study, ATDC5 cells were induced by lipopolysaccharide (LPS) to establish an AS inflammatory injury model. The expression levels of FGF21 and KLF4 were detected using reverse transcription‑quantitative PCR and western blotting. Cell transfection was performed to alter the expression levels of KLF4 and FGF21. Subsequently, the regulatory effects and mechanisms underlying KLF4 and FGF21 on oxidative stress and inflammation in AS were investigated by performing Cell Counting Kit‑8 assays, ELISAs, TUNEL staining and western blotting. Moreover, the expression levels of sirtuin 1 (SIRT1)/NF‑κB/p53 pathway‑related proteins were detected via western blotting. FGF21 overexpression promoted LPS‑induced viability on ATDC5 cells, inhibited LPS‑induced apoptosis, and decreased the LPS‑induced inflammatory response and oxidative stress levels of ATDC5 cells. Overexpression of the transcription factor KLF4 reversed the protective effect of FGF21 overexpression on LPS‑induced inflammatory injury in ATDC5 cells. The results suggested that this process may be achieved via regulating the SIRT1/NF‑κB/p53 signaling pathway. Overall, the present study demonstrated that KLF4 downregulates FGF21 to activate inflammatory injury and oxidative stress of LPS‑induced ATDC5 cells via SIRT1/NF‑κB/p53 signaling.
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